BSc Nutrition @ Kingston University

Now that you’ve read part 2….(you have read parts 1 and 2 right?)

We need to shift the focus of the blame game from the individual. We can’t continue waiting to see what individuals will do, we need to steer them. And a nudge is not sufficient, people need a push (the Government seems to prefer a gentler and cheaper and less controversial nudge)! We need political commitment, collaboration of public and private stakeholders (governments, international partners, civil society and nongovernmental organizations and the private sector). Undoubtedly, all these play major roles in shaping healthy environments and making healthier diet options affordable and easily accessible. It is undeniable that changes by the food industry could accelerate health gains worldwide. In what way? Reducing fat, sugar and salt content of processed foods and portion sizes, introducing innovative, healthy, and nutritious choices, and reviewing current marketing practices.

An interesting read in this matter comes from a series of papers looking at “Lessons from Tobacco Control for the Obesity Control Movement”. Tobacco and obesity? Think about it. “Both public health problems share common elements of “false consciousness” (“smoking/obesity is simply the result of the consumers’ free choices”) and a powerful industry whose interests are best served if consumers smoke/overeat.”. What we need is a shift away from individual risk factors to the creation of an atmosphere conducive to health (as opposed to an environment that promotes obesity – “obesogenic” environment or smoking).

But how do you do that? Governments may need to implement radical policy change, to regulate food consumption and control food industry in a similar way to that of tobacco industry, by banning advertising of selected produce, taxing certain foods, and rationing purchase/restricting availability of certain types of food or opportunities to eat (in particular, foods targeted to children). Side by side to this, we obviously also need to provide information about how to avoid over-eating, increase concern about the adverse effects of over-eating, provide treatment for over-eating, and reducing the social acceptability of over-eating or eating too much of particular kinds of food.

But how can a Government, any Government, justify this? McCormick et al (2007) attempts to provide a rationale for government intervention. It proposes four drivers of Government intervention: externalities (the individual does not bear the full costs of obesity, society does, e.g. NHS), imperfect information (“If individuals do not fully understand or accurately perceive the risks and consequences of their choices regarding diet, exercise and weight, they may make decisions that do not maximize their welfare”), vulnerable individuals (there is clear unquestionable evidence that patterns of food consumption and exercise are set early in life – this puts in a strong case for government intervention in preventing childhood obesity) and time-inconsistent preferences (“a situation in which an individual’s preferences change over time without any change in information; for instance, intending to drink only three pints at the pub but drinking more when you get there”).

However, draconian action of this kind would be considered disproportionate and politically unacceptable. Some of the most intrusive options available will only really become an option “if observable patterns of over-eating come to be viewed by the public as illegitimate, thus meriting tough action to control them”. This means that most politicians would consider such actions as potential political suicide (particularly as in the space of a 5 year Parliament it may be difficult to see the benefits of such interventions…and thus re-election). Talks of an attack on free choice and nanny state would certainly follow. Imagine the outburst of the daily newspapers….And then food is not tobacco. We need food but we clearly don’t need tobacco. This just makes the problem even more complex. Then again, what was the situation with tobacco 40 years ago? How much have we changed? In the developed world, we’ve reduced smoking prevalence by almost half through taxation of tobacco products, smoking bans in public places, laws prohibiting tobacco sales to minors, advertising restrictions, and aggressive public education campaigns. “Public health interventions to decrease obesity prevalence must apply the same kind of multifaceted and coordinated approach that reduced tobacco use in order to change individual behavior patterns and effectively address the environmental barriers to physical activity and healthful food choices.”

What do the years ahead look like? The October 2007 Foresight report, Tackling Obesities: Future Choices project predicted that 60% of men, 50% of women and 25% of children could be obese by 2050 and that the overall costs to society could climb up to 40-50 billion (depending on which statistician is right) by 2050 if nothing changed between now and then. This compares to the current estimate of 16 billion (NHS direct costs and other costs to society and the economy (e.g. sickness absence reduces productivity)). Can the NHS budget resist such an aggression? Can we afford to spend 16 billion pounds every year (and increasing) on treating obesity and its consequences? Are we not going through a financial crisis? Who is going to pay for consecutive Governments’ failures to choose and enforce the most cost-effective measures to save us from this “obesogenic” environment? Yes, you’ve guessed it. Tax payers…

Did you read part 1? Read it first (scroll down)….otherwise, carry on.

To reduce the burden of obesity at a population level, we need to get people who are overweight and/or obese to consume fewer calories or to increase energy expenditure. Ideally both. Even better, we want to prevent them from becoming overweight in the first place (it stands to reason, that if you don’t become overweight, you can’t become obese). The main focus of any intervention should thus be on “preventing small excesses of weight, which lead to large weight gain over time, as once a large amount of excess weight is gained, it is very difficult to lose”.

We assume that informed consumers will use all the information we provide them about the benefits of a healthy diet and lifestyle and act accordingly. After all, don’t we all want to be healthy? Achieve energy balance and a healthy weight, limit energy intake from total fats (and from saturated fats to unsaturated fats), increase consumption of fruit and vegetables, as well as legumes, whole grains and nuts, limit the intake of sugars, increase physical activity (at least 30 minutes of regular, moderate-intensity activity on most days). It falls on the individual to change diet and lifestyle for all to be well. BUT attempts to decrease obesity that focus primarily on changing individual behaviour have been mostly ineffective on a population level (as Part 1 of this piece has shown us). Knowledge alone may be insufficient to induce sustained changes in dietary habits. Obviously, we need to promote health. No one believes that an individual will act if he/she has no information or does not know how and what to do in order to change. No knowledge means no support for Government action perceived to be more intrusive (“I do not know why you are doing this and hence I will not accept it”). And, most importantly, this information must come from reliable sources. Do not despair. We do need nutritionists! However, we can’t rely solely on education, persuasion, facilitation, upskilling or empowerment (powerful as they may be). We need new strategies. Onwards to Part 3…

Obesity is on the news every day. We hear about how bad it is, that it is getting worse, that it has taken epidemic proportions and is the new pandemic of the XXI century, that this will lead to a “tsunami” of type 2 diabetes and cardiovascular disease…etcetera etcetera. We spend tons of money trying to shed the extra kilograms. Americans alone spend up to $60 billion dollars per year on weight-loss programs and products. The UK market was estimated to be worth £11.2bn in 2007. Yet, for all the money we throw at it, here or in the States (and probably in most developed nations for that matter), 50% of any weight loss is regained within one year and most, if not all, is regained within 5 years. In 2004, the House of Commons Select Committee estimated the total annual cost of obesity and overweight to be around £6.6–7.4 billion per year.

Let’s get a quick snapshot of the UK. It’s not a surprise to anyone that, as a country, we are getting bigger. According to the latest National Diet and Nutrition Survey, the average BMI for men and women (19-64y) was 27.5 and 27.0 Kg/m2, respectively. 68% of men were overweight or obese (27% obese) whilst 55% of women were overweight or obese (25% obese). Half of the “just” overweight population is likely to become obese. 34% of males and 42% of women had a very high waist circumference (meaning greater than 102cm for men and 88cm for women). What this translates into is a much greater risk of chronic disease (e.g. metabolic syndrome, diabetes type 2, and cardiovascular disease/events such as coronary heart disease and risk of stroke and myocardial infarction). The picture is not much different in those aged 2 to 18 years of age where 33-34% of all boys and girls are now overweight and/or obese (for obese only: 18-19%). 50% of obese children at age 6 become obese adults.

How quickly have things changed? For this we need to look at the latest Health Survey for England 2009 published December 2010. From 13% of obese man and 16% of obese women in 1993, we’ve gone up to 22% and 24% in 2009, respectively. Simultaneously, the proportion of individuals with a raised waist circumference increased in males from 20% in 1993 to 32% in 2009 and in women from 26% to 44%. The UK National Institute of Health and Clinical Excellence (NICE) recommends that we assess the health risks associated with overweight and obesity by combining BMI with waist circumference in adults. What this equates to is that the proportion of men at high risk of chronic disease increased from 11% in 1993 to 14% in 2009, while for women the proportion increased from 12% to 18%. A much steeper rise can be seen for the high risk category with an increase from 11% to 20% for men and 14% to 23% for women.

Is it just the UK? No but we are one of the worst in Europe (original paper here). British women now have the 3rd highest BMI out of 23 European Nations (up from 12th in early eighties – BMI went up from 24.2 to 26.9 kg/m2) whilst men now have the 5th highest BMI (up from 17th position; BMI increased from 24.7 to 26.6). How do we change this? Onwards to Part 2.

According to a recently published study (download full paper here) on the prestigious Archives of Internal Medicine (a scientific peer reviewed journal), “in older women, several commonly used dietary vitamin and mineral supplements may be associated with increased total mortality risk”.

So, what exactly did the authors find? They found that in older women (mean age 61.6 years at baseline in 1986) participating in the Iowa Women’s Health Study the absolute risk of dying was increased over the 22 year study by 2.4% for those taking multivitamins, 4.1% for vitamin B6, 5.9% for folic acid, 18% for copper, 3.9% for iron, 3.6% for magnesium and 3.0% for zinc all when taken as a supplement. There was, however, a 3.8% reduction in the absolute risk of mortality when taking calcium supplements. Also, of interest, the risk of dying increased with increased supplemental iron, so the more you took, the higher the risk of dying. With calcium, its suggested protective effect was lost at higher doses (the authors found a reduction of the risk of dying with supplemental doses of up to 1300 mg/day with the protective effect disappearing with daily doses higher than 1300 mg/day). This was also reported on the news here and here and here but also on science related news sites such as here here and here.

This study has in its favour the size of the sample studied (38 772 women), the longitudinal repeated measures design with use of dietary supplements queried 3 times – at baseline in 1986, 1997, and 2004 (this reduced the risk of incorrectly describing use of supplements) and an average follow-up time of 19 years. In addition, the authors also adjusted their analysis for age; educational level; place of residence; diabetes mellitus; high blood pressure; body mass index; waist to hip ratio; hormone replacement therapy; physical activity; smoking status; and intake of energy, alcohol, saturated fatty acids, whole grain products, fruits, and vegetables. I will explain what this means later on.

The authors also highlighted, quite rightly, some limitations:

1) Being diagnosed with e.g. cancer or cardiovascular disease during follow-up may increase use of supplements (these people then die earlier because of the condition and not because of the use of supplements). What did the authors say about this? They did not find evidence, on this cohort, that having CVD, diabetes of cancer prior to the baseline measure increased use of supplements later on. In addition, for those diagnosed with cancer during the study, no evidence of increased use of supplements was found. As mentioned above, the authors adjusted their analysis for diabetes mellitus; high blood pressure; body mass index; waist to hip ratio; physical activity; and smoking status (amongst other variables).

Why? To exclude the impact of these factors on the estimate of risk of mortality. In other words, after some complicated statistical analysis (I will not bore you with that…), they wanted to be able to say that the differences found, if any, for the mortality risk between the group taking the supplements versus the group not taking the supplements were not due to one of the groups having more cases of diabetes, hypertension, obesity, or having more people physically inactive or smoking.

You want to limit the impact of a number of different variables that may explain the differences in mortality rate across the two groups so that any differences found may possibly be explained by the variable you are actually interested in, i.e., use of supplements vs. non-use of supplements. So, all these extra factors act as potential confounders. By adjusting for these potential confounders that are known to affect survival, one may actually increase the precision with which one can estimate the effect of giving supplements.

So, going back to the results highlighted earlier in this piece, the authors found that the absolute risk of dying was increased by 2.4% for use of multivitamins after adjustment for the other explanatory variables in the model. So, by removing the impact of the other variables known to impact on risk of dying for which data were available, one was still left with a statistically significant increase risk of dying of 2.4%. May seem very small but it’s there.

2) Those taking supplements may be the least likely to need them. Dietary supplement users tend to have underlying diets (and lifestyles) that are healthier. Those taking supplements may be the least likely to need them, the so-called “worried well”. This healthier lifestyle should, in theory, result in a reduction of risk of chronic disease and premature death. So, in the same sense that you have to adjust for diabetes or hypertension, you also have to adjust for these healthier lifestyle variables.

3) The nature of the statistical analysis performed requires that the p value be dropped for every variable you adjust for. As there were 15 variables, the p value dropped to 0.05 / 15 = 0.003. What does this mean? This means that the authors could not just be satisfied with being 95% sure that the difference found in regards to risk of mortality was a true difference and not just something that happened by chance. They had to be 99.7% sure that the difference did not occur by chance. However, they did not achieve this for all the variables tested – this level of certainty was only achieved for multivitamins, copper, and calcium.

The authors concluded by saying that “in this large prospective cohort of older women, we found that most dietary supplements were unrelated to total mortality rate. However, several commonly used dietary vitamin and mineral supplements were associated with increased total mortality rate, most strongly supplemental iron; calcium showed some evidence of lower risk.” A very important message from this paper, also highlighted by the authors, was that association does not equal causation. The authors never said that supplement use was the cause of increased mortality. What they said was that use of some supplements was associated with increased mortality, meaning both variables were present at the same time but you cannot establish whether one led to the other. This is an obvious conclusion as this study is an observational study.

This study raised concerns about the long-term safety of various vitamin and mineral supplements. Whilst there is undoubtedly a lot of supporting evidence for the use of supplements to address nutritional deficiencies, the case for using them with a goal of achieving health benefits beyond those achieved by a healthy diet is not established (what some people refer to as optimum nutrition – even if the concept of optimum nutrition cannot be defined biologically – how do you know you have achieved it if there is no definition, criteria or test for optimum nutrition?). We do not know what the implications are of the long term intake of supplements that exceeds the upper recommended levels of intake. Do they bring any benefit? Most importantly, do they do no harm?

A significant number of people take supplements in supra-physiological doses, far in excess of the levels found on the Dietary Reference Values book or the guidance set by the Expert Group on Vitamins and Minerals (Food Standards Agency, 2003) in its publication entitled “Safe Upper Levels for Vitamins and Minerals”. In these instances they act as drugs. For a drug to come on the market, they need to go through a rigorous and very long process of safety testing before it is allowed to be put on the market. However, “Dietary supplements, unlike drugs, do not require rigorous RCT testing, and observational studies are often the best-available method for assessing the safety of long-term use”. So why do we take and accept them so light heartily?

Take away messages summarised from here
1) “More is not always better”
2) “The truth that we need to change our eating and exercise habits is harder to swallow than a supplement pill”
3) “Supplements can help some people, harm others, and have no effect on most”
4) New nutrients aimed at your money, not your health à there are no magical nutrients

PS. In 2009, sales of dietary supplements in the UK totalled £670 million pounds. At the top of the list you could then find multivitamins and fish oils (close to £140 million each).

PS2. You are all doing a Bachelor of Science. This means that you will become scientists by the end of your degree. Remember, science should always be objective and unbiased. Remember that when you read comments posted on newspapers websites or if you come across some potentially “biased” websites. Not many topics generate such fervid debate as the use of supplements and what these can theoretically do. Dismissing a scientific paper simply because you do not agree with it or because you don’t like its findings (supplements may do harm) and then accepting another paper because it supports your views (supplements may do good), not reading a paper and then making wide assumptions about it, reading a paper with the intent of finding something to dismiss it….none of this is science. So, don’t do it!

You may have already come across this in the scientific literature (and the media). Lack of sleep may increase your risk of obesity. For example, Bell and Zimmerman (2010) showed that for infants and pre-school aged children, their risk of overweight/obesity was increased by 80% (or increased by 1.8 times) if they slept for less time. In addition, trying to make up lost night time sleep with day napping did not reduce risk

Another more recent study Carter et al (2011) also showed that longer sleep duration at age 3-5 was associated with a reduction in BMI (0.48 for each extra hour of sleep) and a 61% reduction in the risk of being overweight at age 7. Lack of sleep manifested itself via increased fat deposition. An editorial on the same journal by Cappuccio and Miller (2011) provides a nice short summary.

Move onwards towards adolescence. Olds et al (2011) compared Early-bed/Early-rise vs. Late-bed/Late-rise adolescents and found that the latter were 1.47 times more likely to be overweight or obese, 2.16 times more likely to be obese, 1.77 times more likely to have low moderate-to-vigorous physical (they did, on average, 27 min less moderate-to-vigorous physical activity), and were 2.92 times more likely to have high screen time (they watched, on average, an extra 48 min/d more screen time). Interestingly, both groups slept for similar amounts of time. This suggests that the time of the day when we sleep is important (it is not just about total sleep time).

So, how does not sleeping “help” you gain weight? Two possibilities: you either increase energy intake through not sleeping (so more opportunity/time for eating/snacking) and/or reduce energy expenditure (during the day as a whole because of tiredness and compensating mechanisms). A short commentary by Chaput (2010) in the appropriately named Sleep journal offers several explanations on how lack of sleeping contributes to weight gain. Prominently, he suggests that short sleep duration promotes overconsumption of food via a reward-driven eating behaviour (hedonistic – meaning it is associated with an increased use of food as a reward or source of pleasure). Overall, this potentially contributes to overconsumption of food “in the absence of hunger”.

Why does this matter? This matters because early life sleep patterns may carry through from infancy to childhood, adolescence and adulthood and so become yet another established risk factor for overweight and obesity in adulthood (in excess of 50% of obese adolescents become obese adults). Morale of the story: “Sleep is not a waste of time”.

Interestingly, a trial by Cizza et al (2010) started last year in the US, where they are looking at treating obesity by extending sleep duration (via a randomized, prospective, controlled trial). This 4 year trial will be looking at the impact of increasing sleep duration (from less than 6.5 hours to a healthy 7.5 hours) on body weight, endocrine (leptin and ghrelin) and immune (cytokines) parameters, the prevalence of metabolic syndrome, body composition, psychomotor vigilance, mood, and quality of life. Will this be another weapon in the fight against obesity?

Needed an excuse to sleep more? There you go. I’m going to sleep on that.

No, not Brussels sprouts. Yes, you’ve got it. Chocolate! An interesting editorial came out on the British Medical Journal (BMJ) on the 20th September 2011 entitled “The temptations of chocolate”. This was a short comment on another paper published in the BMJ by Buitrago-Lopez et al. (2011) entitled “Chocolate consumption and cardiometabolic disorders: systematic review and meta-analysis”. This was widely publicised in the news as well.

The authors identified 7 studies (all observational, though) involving a total of 114 009 participants which met the inclusion criteria for the meta-analysis. So what did they find? When comparing those with the lowest intake of chocolate versus those with the highest intake they found that the latter was associated with a 37% reduction in cardiovascular disease (this the same as saying that the relative risk was 0.63 (95% confidence interval 0.44 to 0.90)), a 31% reduction in diabetes and a 29% reduction in stroke. It was not possible to indicate, based upon the available data, what type of chocolate was better.

As you know, I do like to fill my lectures with interesting slides and if it involves graphical display of data for you to interpret, even better. So here is a forest plot.

Figure 1. Relative risks for cardiovascular disease, heart failure, and stroke in adults with higher levels of chocolate consumption compared with lower levels (Buitrago-Lopez et al., 2011).

Confused? The vertical line represents no effect. To the left is reduced risk, to the right is increased risk. The diamond shape object represents the aggregate effect of all studies combined. As the diamond shape does not overlap with the line of no effect for studies looking at All Cardiovascular disease, this suggests there is a statistically significant reduction of risk. Of how much? Look at the Relative risk column. Aggregate is 0.63 meaning a 37% reduction in risk.

The authors, based on current knowledge, offered some possible explanations for this reduced risk. Cocoa derived products are rich in polyphenols (antioxidants) and may promote release of nitric oxide by the cells that line the interior of blood vessels (so called endothelium). So? Well, this endothelial nitric oxide protects against atherosclerosis by, e.g., inhibiting platelet aggregation, leukocyte adhesion, smooth muscle cell proliferation, and expression of genes involved in atherogenesis plus potentially additional beneficial effects on blood pressure, insulin resistance, and blood lipids.

Chocolate is a high fat high sugar food with 100g giving you roughly 500 kcal. If the conclusions from this study can be corroborated by randomized controlled trials, then this opens the opportunity for the food industry to reduce the energy density of chocolate whilst maintaining the potential beneficial effects of chocolate.

The authors highlight a series of strengths but also limitations of the review. Make sure you read that section. The main message seems to be not to run off to the supermarket (just yet) for that bar of chocolate! And obviously, despite tempting, this is likely not to be the best way to reduce the risk of chronic disease. Brussel sprouts anyone?

Welcome to the blog page for the BSc Nutrition degree at Kingston University. This blog has been created to highlight recent scientific research, reports or news stories that relate to the field of Nutrition. It is hoped that this blog will complement your knowledge of the subject area. The twitter widget on the right hand side will provide short news bulletins in less than 140 characters to those stories.

If you scroll down this page, you will be able to read some posts relating to a Level 6 module entitled Nutrition in Developing Countries (HC3010). These were written as part of a wider project looking at the potential of blogs, micro-blogging (Twitter), and Facebook on the learning and teaching of Nutrition during the 2010/11 academic year. The posts are related to topics discussed as part of that module. They are being kept for historical reasons.

Will Japan’s Crisis Send Food Prices Even Higher? From http://moneywatch.bnet.com/economic-news/blog/daily-money/will-japans-crisis-send-food-prices-even-higher/2300/

Below, you can find a number of reasons why Japan’s earthquake, tsunami and nuclear power plant emergency can lead to higher food prices.

1) Japan already imports about 60% of its food and with 2/12 major ports through which food imports come in destroyed and nuclear plants affected, this means both transport and processing of foods is affected. However, Japan has significant stockpiles of food (some increase in imports is expected but should be short lived – more about this below);

2) Japan only produces 20% of the grain they need (Japan imported 3 billion US dollars of grain yearly just from the US) which happens mostly in the area affected by tsunami. With drop in grain production, Japan may reduce corn and wheat imports and switch to importing cereal (already processed). Rice (an important commodity in Japan – rice consumption is around 10 Kg/month/capita on a usual month) should not suffer PROVIDED they can plant this year’s crop and hoarding does not continue (http://www.bloomberg.com/news/2011-04-12/japan-rice-buying-may-outstrip-supply-on-hoarding-marubeni-s-shibata-says.html). Japan purchased 8 million tonnes of rice in 2010 and there are concerns this may rise to up to 15 million tonnes this year if hoarding rice because of fears/rumours of radiation contamination continues (this was in fact observed soon after the Earthquake leading to a temporary rice shortage). The tsunami also destroyed 18% of the country’s rice production (rice paddy fields flooded with sea water, machinery destroyed). Out of the 8.5 million tons of rice the country produces, 1.56 million tonnes come from Fukushima (affected by radiation) and neighbouring Ibaraki, Miyagi and Iwate (affected by tsunami) prefectures. All this may further boost imports to make up for shortfall (and add to speculative pressure). Having said that, the country’s rice stockpiles of around 3 million tonnes should cover almost five months of consumption. Imports of wheat may also increase if hoarding of rice exceeds import capacity although Japan still expects imports of wheat to go down from 5.39 million tons last fiscal year (highest level in past 6 years) to 5.11 million tons of food wheat in the year to March 31, 2012. http://www.bloomberg.com/news/2011-04-12/japan-rice-buying-may-outstrip-supply-on-hoarding-marubeni-s-shibata-says.html;

3) Japan imports 100% of pork and 75% of beef.

4) There are concerns regarding increases in prices for sushi (damaged ports – we all saw the pictures of fishing boats stranded in land – where is all that sushi coming from now?) and Kobe beef; Japan also has substantial exports of fruits, vegetables, dairy products and seafood (30% of Japan’s annual seafood harvest exported just to US; Japan exports around 200,000 tonnes of seafood per annum in total, according to the WHO); in 2009, in excess of 70% of Japan’s food exports went to Hong Kong, the U.S. (Japan accounts for 4% of American food imports – http://www.nytimes.com/2011/03/19/business/global/19radiate.html?_r=1), China, Taiwan and South Korea (source: Japan External Trade Organization); Japan exported 481 billion yen of food in 2010 (3.5 billion pounds), accounting for 0.7% of its total exports – http://foodsafety.suencs.com/archives/tag/contamination-of-japanese-food-export)

5) There are also concerns about radioactive contamination (Fukushima nuclear plant) of water and food, with some countries, e.g. China and South Korea testing foods and restricting food imports from Japan – http://www.theglobeandmail.com/news/world/asia-pacific/radioactive-contamination-of-japanese-food-serious-who/article1949643/. The EU is also looking at radiation contamination checks on imports of Japanese food products (above and beyond tests already done in Japan) http://www.internationaltradesolutions.co.uk/all-news-articles/311-eu-instigates-radiation-contamination-checks-on-imports-of-japanese-food-products and http://www.bbc.co.uk/news/business-12815906. This has resulted in Japan urging calm over food exports http://www.reuters.com/article/2011/03/30/us-japan-food-exports-idUSTRE72T77D20110330;

6) Last but not least, speculators may place upward pressures on food prices presuming the potential added pressure on the global food supply.

On a separate note, some people also started hoarding iodized salt (this is because iodised salt also has potassium iodide) in the belief this would protect them from radiation although this is not the case. There is a recommendation, in radiation emergencies, to take potassium iodide tablets before exposure to radiation to reduce accumulation of iodine in thyroid gland http://worldblog.msnbc.msn.com/_news/2011/03/18/6294237-chinese-hoard-salt-out-of-radiation-fears; you can find out more about how potassium iodide works by visiting the US Centers for Disease Control and Prevention (CDC) at http://emergency.cdc.gov/radiation/ki.asp and also from http://www.health.harvard.edu/blog/potassium-iodide-pills-and-prevention-of-thyroid-cancer-from-japanese-nuclear-power-plant-201103141864 or http://www.doh.state.fl.us/environment/radiation/KI-Fact-Sheet.pdf.

But what do Potassium Iodide tablets do and why does iodised salt offer no protection?

Assuming 130 micrograms of potassium iodide per 1.5 grams of iodised salt, one would need to take 1.5kg (1,500g) of salt per day to reach 130 MILLIGRAMS of Potassium Iodide (what one adult dose tablet contains). Even as little as an extra 6 g of salt on top of someone’s salt intake will result in adverse cardiovascular effects even in young normotensive individuals (see http://www.ncbi.nlm.nih.gov/pubmed/18458163). 1.5kg of salt would be potentially lethal. Potassium iodide pills should only be taken in emergencies (as continuous use is dangerous). The Potassium iodide when taken before exposure saturates the thyroid gland and prevents it from absorbing the radioactive iodide for the next 24 hours (“byproduct of the fission (splitting) of the uranium in the fuel rods that power a nuclear power plant”). It is in the thyroid gland that this radioactive iodine accumulates and increases risk of cancer – http://www.health.harvard.edu/blog/thyroid-cancer-a-hazard-from-radioactive-iodine-emitted-by-japans-failing-nuclear-power-plants-201103141867).

Japan is one of the biggest aid donors across the world. E.g. see http://www.devex.com/en/blogs/the-development-newswire/japan-makes-record-donation-to-wfp (“The World Food Program has thanked Japan for its donation of USD196.6 million, the largest-ever single contribution received by the U.N. agency…”).

There is little information at present (at least that I could find) regarding the humanitarian response in what relates to food. What exactly is being shipped to Japan/given to people? From the news we know that “Millions of people spent a third night without water, food or heating in near-freezing temperatures along the devastated northeastern coast“, “People are surviving on little food and water…“, “…authorities were receiving just 10 percent of the food and other supplies they need…” and “The government has sent 100,000 troops to spearhead the aid effort. It has sent 120,000 blankets, 120,000 bottles of water and 29,000 gallons (110,000 liters) of gasoline plus food to the affected areas“. (from http://news.yahoo.com/s/ap/ap_on_bi_ge/as_japan_earthquake).

The Government seems to be considering “the possibility of delivering food by sea or air, given the problems with roads en route to the north“ (from http://www.washingtonpost.com/wp-dyn/content/article/2011/03/13/AR2011031300977.html).

It seems there is some food distribution taking place already with people “calmly (queueing) for food baskets, while the shelves of convenience stores were stripped bare….” Gaining access to medication may also be difficult (from http://news.yahoo.com/s/afp/20110313/wl_asia_afp/japanquakedevastation).

Despite a different scenario, one can find much more information in regards to the humanitarian response following the 26th December 2004 Sumatra-Andaman earthquake earthquake and Indian Ocean tsunami which resulted in the death of an estimated 230,000 people in fourteen countries (including Indonesia (hardest hit), Sri Lanka, India, and Thailand). It was the third largest earthquake ever recorded (9.1-9.3 Richter scale: max 10), one of the deadliest natural disasters in recorded history (http://www.cbc.ca/news/world/story/2008/05/08/f-natural-disasters-history.html) and perhaps the world’s largest relief and recovery operation to date.

From http://www.undp.org/cpr/disred/documents/tsunami/indonesia/sr13.pdf we can note that “Food: WFP reported that the warehousing capacity in Banda Aceh for
1,600 MT. The food basket for Banda Aceh and Aceh Besar will consist of rice, noodles, oil with the possibility of fish. Current stocks include 1,300 MT rice, 170 MT noodles, and 70 MT of biscuits. Distribution began on 4 January, with approximately, 102 MT. Full scale distribution is anticipated across Aceh Province within 10-14 days. WFP and TNT now has 40 trucks running convoys between Medan and Banda Aceh. Food is also dispatched to Singkil for distribution in the West Coast area. …………………………….9. WFP has so far dispatched 1,309 MT of food commodities and expects to complete the distribution of a one-month ration to 130,000 IDPs in Banda Aceh and Aceh Besar within the next few days. Helicopters are now distributing 15 MT on a daily basis to communities on the most affected west coast. WFP food (fortified biscuits and rice) was distributed to the west coast (Calang and Meulaboh) with the help of the U.S. Air Force and to islands off the coast by ferry.”

From http://www.fas.org/sgp/crs/row/RS22027.pdf we can note that WFP’s initial response to the disaster “…was to provide immediate food assistance in the affected countries over a two- to three week period following the disaster. Using available funds ($1.9 million), WFP provided food to an estimated 600,000 people. Where available, WFP purchased local food, but fortified foods were quickly airlifted to the region. Food stocks in the various countries destined for WFP development projects were reallocated to emergency relief. WFP shipments on the high seas were diverted to countries affected by the disaster.”

WFP then made an appeal for $185 million to purchase 169,000 metric tons of food to feed 2 million people over six months (January to June 2005). This included 126,000 MT of rice, 7,500 MT pulses, 2,700 MT sugar, 9,450 MT canned fish, 6,500 MT vegetable oil and 17,300 MT fortified foods (biscuits, noodles, and blended foods). (“…Targeted beneficiaries, according to WFP, are poor and vulnerable people already living in extreme poverty. They include displaced people, those who lost their houses and/or means of livelihood and other productive assets, and children who lost parents and families.”

It is also important to note that at the time of the Indian Ocean disaster there was already a very high demand for emergency food aid to respond to urgent needs (mostly targeted at sub-Saharan Africa). If calls for further aid do not get the desired response or there are (expected) delays, Governments may (and are) sometimes (be) forced to reassess distribution priorities of both emergency and non-emergency food aid (or aid in general) – same pot of aid for more people.

First we had the food crisis, then the world economic crisis and now another food crisis. The FAO Food Prices Index is at its highest level since 1990, when it was first used. This means it is now highest than at the last food crisis peak in June 2008. Various reasons have been put forward to explain this rise including rising production costs, growing demand from biofuels and a rapidly-expanding population (which obviously needs more food). This may once again push the number of hungry people to above 1 billion (like it happened in 2009 after the last food crisis).

Want to know more? click on http://online.wsj.com/article/SB10001424052748703386704576185944194748916.html